POS0324 OBESITY IS A RISK FACTOR FOR POOR RESPONSE TO TREATMENT IN EARLY RHEUMATOID ARTHRITIS - A NORD-STAR SPIN-OFF STUDY
Authors: V. Dubovyk, G. Gröndal, B. Gudbjornsson, E. A. Haavardsholm, M. Heiberg, M. L. Hetland, K. Hørslev-Petersen, M. C. Kapetanovic, A. Kastbom, J. Lampa, K. Lend, D. Nordström, M. Nurmohamed, M. Rizk, A. Söderbergh, T. Uhlig, M. Østergaard, R. Van Vollenhoven, A. Rudin, C. Maglio
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Several therapeutic options are currently available to treat rheumatoid arthritis (RA); however, the response to treatment is highly variable, and not all patients achieve clinical remission [1]. Obesity is suggested to lower the chances of remission [2], even though a recent observational study has shown that obesity is not associated with reduced response to conventional synthetic anti-rheumatic drugs in patients with early RA [3]. <h3>Objectives</h3> The aim of this study is to determine if obesity affects the response to treatment in participants with early RA. <h3>Methods</h3> This report includes 393 Swedish patients from the NORD-STAR study, which is a multicenter, randomized trial on 812 patients with untreated early RA [4]. The 393 participants have been randomized at baseline into 4 arms of treatment: methotrexate combined with (1) prednisolone, (2) certolizumab, (3) abatacept, or (4) tocilizumab. Scores for disease activity and blood samples were measured and collected before randomization and at 24-week follow-up. Multiple linear regression and binary logistic regression analyses were performed after adjustment for sex, baseline age, anti-citrullinated peptide antibody status, current smoking, disease activity score- C-reactive protein (DAS28-CRP), and treatment randomization. The outcomes for this report were: DAS28-CRP ≤3.2 (DAS28-CRP low disease activity), DAS28-CRP ≤2.6 (DAS28-CRP remission) and clinical disease activity index (CDAI) ≤2.8 (CDAI remission). <h3>Results</h3> In total, 75 (19%) participants had obesity at baseline, defined as body mass index (BMI) ≥30 kg/m<sup>2</sup>. The percentage of patients with obesity in each treatment group was (1) 25%, (2) 15%, (3) 19% and (4) 19%. At baseline, there were no differences in terms of disease activity indices and inflammation parameters between patients with BMI &lt;30 vs. ≥30 kg/m<sup>2</sup>, except for the number of swollen joints (SJC28), which was slightly lower in those with obesity (mean+SD, 8±5 vs. 9±5, <i>p</i>=0.018). At 24-week follow-up, patients with obesity had higher disease activity indices and inflammation parameters compared to patients with lower BMI (Table 1). Moreover, patients with obesity had a lower chance of achieving response to treatment as measured by DAS28-CRP ≤3.2 (OR 0.5, 95% CI 0.2 - 0.9, <i>p</i>=0.025), DAS28-CRP ≤2.6 (OR 0.4, 95% CI 0.2 - 0.6, <i>p</i> &lt;0.001) and CDAI remission (OR 0.4, 95% CI 0.2 - 0.8, <i>p</i>=0.006), compared to patients with lower BMI (Figure 1). BMI-treatment interaction was not significant for any score of disease activity. <h3>Conclusion</h3> In patients with early RA, obesity was not associated with higher disease activity before treatment initiation. However, 24 weeks after treatment, patients with obesity had higher disease activity and lower chances to respond to therapy compared to patients with lower BMI irrespective of treatment. <h3>References</h3> [1]Smolen, J.S., et al., Ann Rheum Dis, 2022. doi: 10.1136/ard-2022-223356 [2]Liu, Y., et al., Arthritis Care Res (Hoboken), 2017. doi: 10.1002/acr.22932. [3]Dey, M., et al., Rheumatology (Oxford), 2021. doi: 10.1093/rheumatology/keab389. [4]Hetland, M.L., et al., BMJ, 2020. doi: 10.1136/bmj.m4328. <h3>Acknowledgements</h3> We would like to acknowledge the NORD-STAR Study group. <h3>Disclosure of Interests</h3> Violetta Dubovyk: None declared, Gerdur Gröndal: None declared, Björn Gudbjornsson Speakers bureau: Novartis and Nordic-Pharma, Consultant of: Novartis, Espen A Haavardsholm: None declared, Marte Heiberg: None declared, Merete Lund Hetland Grant/research support from: Research grants from Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Kim Hørslev-Petersen: None declared, Meliha C Kapetanovic: None declared, Alf Kastbom: None declared, Jon Lampa: None declared, Kristina Lend: None declared, Dan Nordström: None declared, Michael Nurmohamed: None declared, Milad Rizk: None declared, Annika Söderbergh Consultant of: Roche, Grant/research support from: Roche, Till Uhlig Consultant of: Consultant for Pfizer and UCB., Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Galapagos, Gilead, Hospira, Janssen, MEDAC, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB., Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Galapagos, Gilead, Hospira, Janssen, MEDAC, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Grant/research support from: Mikkel Østergaard has received research grants from Abbvie, BMS, Merck, Novartis and UCB, Ronald van Vollenhoven Speakers bureau: Speaker, for which institutional and/or personal honoraria were received: AbbVie, AstraZeneca, BMS, Galapagos, GSK, Janssen, Pfizer, UCB., Consultant of: Consultancy, for which institutional and/or personal honoraria were received: AbbVie, AstraZeneca, Biogen, BMS, Galapagos, Janssen, Pfizer, UCB., Grant/research support from: Research Support (institutional grants): BMS, UCB. Support for Educational programs (institutional grants): MSD, Novartis, Pfizer, Roche, Sanofi, UCB , Anna Rudin: None declared, Cristina Maglio: None declared.